RESUMO
Background Perfluorinated alkyl substances (PFAS) are a class of synthetic organic fluorides, which have adverse health effects on brain function, and limited research has been conducted on their effects on depression. Objective To assess potential correlation between serum PFAS and depression. Methods Using the 2015—2016 and 2017—2018 National Health and Nutrition Examination Survey (NHANES) datasets, 2626 subjects with complete relevant information in people ≥20 years old were selected. Logistic regression and restricted cubic splines were used to analyze the association and dose-response relationship between serum PFAS concentration and depression. Subgroup analysis was performed on sex, age, race, education level, marital status, family income to poverty ratio, moderate exercise, body mass index, and drinking status. Results Among the 2626 subjects, there were 666 patients (25.4%) with mild or above depression. After adjusting for race, education level, marital status, body mass index, moderate exercise, drinking history, cotinine, and other types of PFAS, serum perfluorooctane sulfonate (PFOS) was positively associated with the risk of depression (OR=1.85, 95%CI: 1.14, 3.02), and showed a nonlinear dose-response relationship (χ2=6.37, Pnonlinear=0.012). Perfluorononanoic acid (PFNA) was inversely associated with the risk of depression (OR=0.23, 95%CI: 0.14, 0.39), and showed a linear dose-response relationship (Ptrend<0.001, χ2=35.13, Poverall<0.001). After subgroup analysis, it was found that males, 20-39 year-olds and 40-64 year-olds were more sensitive to PFNA exposure (OR=0.15, 95%CI: 0.06, 0.37; OR=0.16, 95%CI: 0.06, 0.40; OR=0.18, 95%CI: 0.08, 0.39). PFOS only showed a statistically significant health effect in people aged 20-39 years (OR=3.00, 95%CI: 1.14, 7.94). In addition, among subgroups of non-Hispanic blacks, cohabitants, current drinkers, high school graduates, and obese patients, exposure to PFAS was significantly associated with the risk of depression. Conclusion PFOS exposure may be associated with increased levels of depression, whereas PFNA exposure may be protective.
RESUMO
<p><b>OBJECTIVES</b>Recently, perfluorooctanoate (PFOA) has been ubiquitously detected in the environment as well as in human serum. Fluorotelomer alcohols (FTOHs), a precursor of PFOA, undergo biodegradation via several metabolic routes which leads to formation of various biodegradation products. The degradation of FTOHs produces an α,β-unsaturated aldehyde that seems possibly to be electrophilic and may react with cellular macromolecules including DNA.</p><p><b>METHODS</b>We investigated the genotoxicity of three FTOHs (6∶2 FTOH, 8∶2 FTOH and 10∶2 FTOH), PFOA and perfluorooctane sulfonate (PFOS) using theumu test.</p><p><b>RESULTS</b>The FTOHs, PFOA and PFOS showed no significant increases in β-galactosidase activity at 0-1000 μM in the absence of S9 mix. The results were unchanged by the metabolic activation with S9 mix.</p><p><b>CONCLUSION</b>The genotoxicities of FTOHs, PFOA or PFOS are not detectable using the present method, suggesting that they are unlikely mutagens.</p>
RESUMO
Objectives: Recently, perfluorooctanoate (PFOA) has been ubiquitously detected in the environment as well as in human serum. Fluorotelomer alcohols (FTOHs), a precursor of PFOA, undergo biodegradation via several metabolic routes which leads to formation of various biodegradation products. The degradation of FTOHs produces an α,β-unsaturated aldehyde that seems possibly to be electrophilic and may react with cellular macromolecules including DNA. Methods: We investigated the genotoxicity of three FTOHs (6:2 FTOH, 8:2 FTOH and 10:2 FTOH), PFOA and perfluorooctane sulfonate (PFOS) using the umu test. Results: The FTOHs, PFOA and PFOS showed no significant increases in β-galactosidase activity at 0−1000 μM in the absence of S9 mix. The results were unchanged by the metabolic activation with S9 mix. Conclusion: The genotoxicities of FTOHs, PFOA or PFOS are not detectable using the present method, suggesting that they are unlikely mutagens.